Long-Acting Thyroid Stimulator
Thyroid Gland
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Thyrotropin
A glycoprotein hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Thyrotropin stimulates THYROID GLAND by increasing the iodide transport, synthesis and release of thyroid hormones (THYROXINE and TRIIODOTHYRONINE). Thyrotropin consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the pituitary glycoprotein hormones (TSH; LUTEINIZING HORMONE and FSH), but the beta subunit is unique and confers its biological specificity.
Graves Disease
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
Polyphloretin Phosphate
Hyperthyroidism
Immunoglobulins, Thyroid-Stimulating
Placental transmission of thyroid-stimulating immunoglobulins. (1/24)
Long-acting thyroid stimulator (LATS) and LATS protector (LATS-P) were assayed at or near delivery in serum from 18 pregnant women with a history of past or present thyrotoxicosis. The results suggested that neonatal thyrotoxicosis may be predicted prenatally if maternal serum LATS and LATS-P concentrations near delivery are above certain levels. (+info)A radio-ligand receptor assay for the long-acting thyroid stimulator. Inhibition by the long-acting thyroid stimulator of the binding of radioiodinated thyroid-stimulating hormone to human thyroid membranes. (2/24)
Highly purified bovine TSH (thyroid-stimulating hormone) was labelled with 125I by using very low concentrations of chloramine-T. Human thyroid membranes prepared by discontinuous sucrose-density-gradient centrifugation were homogeneous on examination by electron microscopy. Incubation of radioiodinated TSH with the membranes showed that radioactivity could be bound to the membranes. Under the experimental conditions described here, binding was dependent on time and temperature and was a saturable phenomenon. Preincubation of the membranes with unlabelled hormone inhibited the subsequent binding of 125I-labelled TSH. Similarly, inhibition by the long-acting thyroid stimulator also showed a saturation behaviour. A rapid and sensitive method for the detection of the long-acting thyroid stimulator is described. (+info)Clinical applications of assays for thyrotropin-receptor antibodies in Graves' disease. (3/24)
Graves' disease is characterized by hyperthyroidism, diffuse goitre, infiltrative ophthalmopathy and, rarely, pretibial myxedema. In 1956 a substance capable of prolonged thyroid stimulation was discovered in the serum of some patients with Graves' disease and termed long-acting thyroid stimulator (LATS). It was shown to be an antibody that could interact with the receptor for thyroid-stimulating hormone (TSH). The term LATS is usually reserved for the activity measured in a laborious in-vivo bioassay in mice. Today the activity of TSH-receptor antibodies (TSH-R Ab) can be measured by in-vitro bioassays or by radioreceptor assays. These assays are now becoming commercially available. TSH-R Ab assays may be useful in predicting the response to therapy for Graves' disease, investigating euthyroid ophthalmopathy and predicting the likelihood of neonatal hyperthyroidism. (+info)Effects of long-acting thyroid stimulator on thyrotropin stimulation of adenyl cyclase activity in thyroid plasma membranes. (4/24)
Both thyroid-stimulating hormone (TSH) and long-acting thyroid stimulator (LATS) stimulated adenyl cyclase activity in plasma membranes obtained from bovine thyroid glands. The stimulation induced by LATS was much less than that obtained with maximal amounts of TSH. LATS inhibited TSH stimulation of adenyl cyclase activity while an equivalent amount of normal human gamma-globulin did not influence basal or TSH-stimulated activity. The inhibition by LATS appeared to be noncompetitive and was greatest when the plasma membranes were initially exposed to LATS for 30 min at 0 degrees C before being incubated with TSH for 10 min at 37 degrees C. Inhibition could still be demonstrated when the plasma membranes were incubated for 30 min at 0 degrees C with TSH before the addition of LATS. Prolonging the period of incubation of plasma membranes with LATS from 30 to 60 min did not augment the stimulation of adenyl cyclase or increase the inhibition of the effect of TSH. Papain digests of LATS also increased adenyl cyclase activity of thyroid plasma membrane and inhibited the stimulation induced by TSH. The inhibitory effect of LATS was not completely specific for TSH and thyroid plasma membranes since glucagon stimulation of adenyl cyclase in hepatic plasma membranes was also inhibited, but to a lesser extent. In contrast to the results obtained with thyroid plasma membranes, LATS did not influence basal adenyl cyclase activity in hepatic plasma membranes. Furthermore equivalent amounts of normal human gamma-globulin also decreased glucagon stimulation of adenyl cyclase activity in plasma membranes obtained from liver. The present data suggest that LATS stimulation of adenyl cyclase in thyroid plasma membranes might be due to a change in the membrane configuration rather than binding to a specific receptor site. Such modification of the membrane structure could interfere with the binding of TSH to specific receptors or to the subsequent stimulation of adenyl cyclase. However, the results do not exclude the possibility that some component in the preparation other than LATS might be responsible for the inhibition of the stimulation by TSH. (+info)The binding of ( 3 H)thyrotropin and an 3 H-labeled exophthalmogenic factor by plasma membranes of retro-orbital tissue. (5/24)
Plasma membranes of cells from retroorbital tissue have been prepared from the Harderian glands of guinea pigs and have been characterized as being reasonably free of other subcellular structures by electron microscopy and by enzyme-marker analyses. Both bovine thyrotropin and a proteolytic derivative of bovine thyrotropin with exophthalmogenic activity but without thyroid-stimulating activity specifically bind to these membranes. Gammaglobulin from the sera of patients with malignant exophthalmos increases the binding of both pituitary factors, whereas binding is not similarly increased by gammaglobulin from the sera of individuals who are not exophthalmic. The increased binding caused by the gammaglobulin from exophthalmic patients is the same whether the sera are positive or negative for the long-acting thyroid stimulator. Present binding experiments do not indicate a direct interaction between the gammaglobulin and the plasma membranes of the cells from Harderian glands. A mechanism for the pathogenesis of human exophthalmos is proposed on the basis of these data. (+info)Thyroid-stimulating activity and chorionic gonadotropin. (6/24)
The nature of the substance with thyroid-stimulating activity (TSA) present in human chorionic gonadotropin (hCG) prepared from pregnancy urine was investigated. In the mouse thyrotropin bioassay, the characteristic maximum of blood radioactivity obtained with the TSA in hCG preparations occurred after that obtained with pituitary thyrotropin (hTSH) but before that obtained with long-acting thyroid stimulator. Antiserum to the alpha subunit of hCG produced significant neutralization of the TSA in hCG. Significant antagonism of hTSH biologic activity was achieved with certain doses of hCG, suggesting that the TSA in hCG was a partial agonist of hTSH. This antagonism was neutralized by antiserum to the beta subunit of hCG. These immunologic results suggest that the substance with TSA in hCG preparations contains antigenic determinants similar to those of both the alpha and the beta subunit of hCG. Amounts of highly purified hCG and crude commercial hCG of equal immunologic activity were biologically indistinguishable in the bioassay for TSA. Both hCG immunoreactivity and the TSA in hCG adsorbed to concanavalin A and eluted with 0.2 M methyl alpha-D-glucopyranoside. These results are consistent with the hypothesis that TSA is an intrinsic property of hCG or of a glycoprotein molecule physicochemically, biologically, and immunologically similar to hCG. (+info)The proteolysis of immunoglobulin G with long-acting thyroid-stimulating activity. (7/24)
1. Proteolysis of immunoglobulin G with long-acting thyroid-stimulating activity with papain and pepsin shortened the duration of thyroid stimulation in mice prepared for the McKenzie (1958) bioassay. The time-course appeared to be related to molecular size. 2. The activity after proteolysis was recovered solely in the electrophoretically slow F(ab)-fragment. 3. There was no immunological cross-reaction between pituitary thyroid-stimulating hormone and the active fragments of the long-acting thyroid stimulator despite their similar behaviour in the bioassay. 4. The implications of these findings are discussed. (+info)Correlation between long-acting thyroid stimulator protector level and thyroid 131-I uptake in thyrotoxicosis. (8/24)
Out of 50 consecutive untreated patients with diffuse toxic goitre 15 showed long-acting thyroid stimulator (LATS), 30 showed LATS protector only, and five showed neither. LATS protector was present in all the patients with LATS. Infiltrative ophthalmopathy was less common in patients with LATS protector only (40%) than in patients with LATS also (67%), but the difference was not significant. There was a correlation between LATS protector level and thyroid (131)I uptake rate factor (k(1)), the coefficient (r) being 0.68 (P < 0.001). LATS level showed no such correlation. The results support the hypothesis that LATS protector is a pathogenic thyroid stimulator in patients with diffuse toxic goitre. (+info)A Long-Acting Thyroid Stimulator (LATS) is an antibody that binds to and stimulates the thyroid stimulating hormone receptor, leading to prolonged and excessive production of thyroid hormones, typically observed in patients with Graves' disease.
A long-acting thyroid stimulator (LATS) is a type of antibody that can stimulate the thyroid gland to produce excess thyroid hormones over an extended period. These antibodies are typically present in individuals with Graves' disease, an autoimmune disorder characterized by hyperthyroidism, goiter, and sometimes eye changes (Graves' ophthalmopathy).
LATS binds to the TSH receptor on thyroid cells, mimicking the action of thyroid-stimulating hormone (TSH) and leading to increased production and release of thyroxine (T4) and triiodothyronine (T3), resulting in hyperthyroidism. The "long-acting" nature of these antibodies distinguishes them from other TSH receptor antibodies, which may have a more transient effect on thyroid function.
The thyroid gland is a large ductless gland located in the neck, responsible for producing thyroid hormones that regulate growth, development, and metabolic rates, as well as controlling heart rate and digestion.
The thyroid gland is a major endocrine gland located in the neck, anterior to the trachea and extends from the lower third of the Adams apple to the suprasternal notch. It has two lateral lobes, connected by an isthmus, and sometimes a pyramidal lobe. This gland plays a crucial role in the metabolism, growth, and development of the human body through the production of thyroid hormones (triiodothyronine/T3 and thyroxine/T4) and calcitonin. The thyroid hormones regulate body temperature, heart rate, and the production of protein, while calcitonin helps in controlling calcium levels in the blood. The function of the thyroid gland is controlled by the hypothalamus and pituitary gland through the thyroid-stimulating hormone (TSH).
Thyrotropin, also known as Thyroid-Stimulating Hormone (TSH), is a glycoprotein hormone secreted by the anterior pituitary gland that regulates the growth and function of the thyroid gland by stimulating the production and release of thyroxine (T4) and triiodothyronine (T3).
Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a hormone secreted by the anterior pituitary gland. Its primary function is to regulate the production and release of thyroxine (T4) and triiodothyronine (T3) hormones from the thyroid gland. Thyrotropin binds to receptors on the surface of thyroid follicular cells, stimulating the uptake of iodide and the synthesis and release of T4 and T3. The secretion of thyrotropin is controlled by the hypothalamic-pituitary-thyroid axis: thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the release of thyrotropin, while T3 and T4 inhibit its release through a negative feedback mechanism.
Graves' disease is an autoimmune disorder that results in the overproduction of thyroid hormones (hyperthyroidism), often characterized by enlargement of the thyroid gland, eye bulging (exophthalmos), and skin changes (pretibial myxedema).
Graves' disease is defined as an autoimmune disorder that leads to overactivity of the thyroid gland (hyperthyroidism). It results when the immune system produces antibodies that stimulate the thyroid gland, causing it to produce too much thyroid hormone. This can result in a variety of symptoms such as rapid heartbeat, weight loss, heat intolerance, and bulging eyes (Graves' ophthalmopathy). The exact cause of Graves' disease is unknown, but it is more common in women and people with a family history of the disorder. Treatment may include medications to control hyperthyroidism, radioactive iodine therapy to destroy thyroid tissue, or surgery to remove the thyroid gland.
Polyphloretin phosphate is a citrus-derived bioflavonoid complex, known for its antioxidant and anti-inflammatory properties, that has been studied in the context of potential benefits for cardiovascular health, capillary integrity, and inhibition of enzymes associated with chronic diseases.
Polyphloretin phosphate is not a widely recognized or established medical term. It appears to be a chemical compound that has been studied in the field of pharmacology and biochemistry, particularly for its potential antioxidant and anti-inflammatory effects. However, it does not have a specific medical definition as it is not a clinically used medication or a standard diagnostic term.
Polyphloretin phosphate is a derivative of polyphloretin, which is a polyphenolic compound found in the bark of trees such as apple and cherry. It has been suggested that this compound may have various health benefits due to its antioxidant properties, but more research is needed to confirm these effects and establish its safety and efficacy in clinical settings.
Hyperthyroidism is a condition characterized by excessive production and release of thyroid hormones from the thyroid gland, leading to an increased metabolic rate and various systemic symptoms like tachycardia, weight loss, heat intolerance, and tremors, among others.
Hyperthyroidism is a medical condition characterized by an excessive production and release of thyroid hormones from the thyroid gland, leading to an increased metabolic rate in various body systems. The thyroid gland, located in the front of the neck, produces two main thyroid hormones: triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating many bodily functions, including heart rate, digestion, energy levels, and mood.
In hyperthyroidism, the elevated levels of T3 and T4 can cause a wide range of symptoms, such as rapid heartbeat, weight loss, heat intolerance, increased appetite, tremors, anxiety, and sleep disturbances. Some common causes of hyperthyroidism include Graves' disease, toxic adenoma, Plummer's disease (toxic multinodular goiter), and thyroiditis. Proper diagnosis and treatment are essential to manage the symptoms and prevent potential complications associated with this condition.
Immunoglobulins, Thyroid-Stimulating (TSI), are autoantibodies that bind to the thyroid-stimulating hormone receptor and mimic TSH activity, leading to hyperthyroidism in diseases like Graves' disease.
Immunoglobulins, Thyroid-Stimulating (TSI), are autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the surface of thyroid cells. These antibodies mimic the action of TSH and stimulate the growth and function of the thyroid gland, leading to excessive production of thyroid hormones. This results in a condition known as Graves' disease, which is characterized by hyperthyroidism, goiter, and sometimes ophthalmopathy (eye problems). The presence and titer of TSIs are used in the diagnosis of Graves' disease.
Thyroid neoplasms are abnormal growths or tumors in the thyroid gland, which can be benign (noncancerous) or malignant (cancerous), and may affect thyroid function and overall health if not treated promptly and appropriately.
Thyroid neoplasms refer to abnormal growths or tumors in the thyroid gland, which can be benign (non-cancerous) or malignant (cancerous). These growths can vary in size and may cause a noticeable lump or nodule in the neck. Thyroid neoplasms can also affect the function of the thyroid gland, leading to hormonal imbalances and related symptoms. The exact causes of thyroid neoplasms are not fully understood, but risk factors include radiation exposure, family history, and certain genetic conditions. It is important to note that most thyroid nodules are benign, but a proper medical evaluation is necessary to determine the nature of the growth and develop an appropriate treatment plan.
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